Infection with Helicobacter pylori increases the risk of gastric cancer. One possible mechanism is the higher likelihood of malignant transformation due to inflammatory responses in the epithelium. An alternative explanation is that these inflammatory responses induce chronic gastritis associated with decreased acidity in the stomach, which in turn increases the endogenous formation of carcinogenic N-nitroso compounds. Inflammatory responses seem to trigger two different causal pathways: one for thediffuse type of gastric cancer and the other for the intestinal type. The striking geographic variability in intestinal gastric cancer can be explained by the synergistic interaction between H. pylori infection and dietary factors, such as intake of salt and ascorbic acid. Screening and eradication of this organism, together with appropriate dietary modifications, offer promise in countries with a high prevalence of H. pylori infection and high risk of gastric cancer, but the safety of such interventions needs to be ensured.